Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD

Rizkallah, Jacques; Man, S. F. Paul; Sin, Don D.

doi:10.1378/chest.08-1516

Cited by 263 publications

(197 citation statements)

References 22 publications

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“…13 A meta-analysis found that the prevalence of PE in acute exacerbations of COPD was 19.9%. 14 Our study identified a small cohort of participants (5.7%) with VTE, which is consistent with some studies with similar prevalence rates. 5,15,16 It should be noted that most studies have examined the prevalence of VTE in the setting of an acute exacerbation, but our cohort reported history of VTE irrespective of exacerbations.…”

Section: Discussionsupporting

confidence: 92%

Risk Factors for Venous Thromboembolism in Chronic Obstructive Pulmonary Disease

Kim¹,

Goel²,

Gangar³

et al. 2014

J COPD F

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Background COPD patients are at increased risk for venous thromboembolism (VTE). VTE however remains under-diagnosed in this population and the clinical profile of VTE in COPD is unclear. Methods Global initiative for chronic Obstructive Lung Disease (GOLD) stages II-IV participants in the COPD Genetic Epidemiology (COPDGene) study were divided into 2 groups: VTE+, those who reported a history of VTE by questionnaire, and VTE−, those who did not. We compared variables in these 2 groups with either t-test or chi-squared test for continuous and categorical variables, respectively. We performed a univariate logistic regression for VTE, and then a multivariate logistic regression using the significant predictors of interest in the univariate analysis to ascertain the determinants of VTE. Results The VTE+ group was older, more likely to be Caucasian, had a higher body mass index (BMI), smoking history, used oxygen, had a lower 6-minute walk distance, worse quality of life scores, and more dyspnea and respiratory exacerbations than the VTE− group. Lung function was not different between groups. A greater percentage of the VTE+ group described multiple medical comorbidities. On multivariate analysis, BMI, 6-minute walk distance, pneumothorax, peripheral vascular disease, and congestive heart failure significantly increased the odds for VTE by history. Conclusions BMI, exercise capacity, and medical comorbidities were significantly associated with VTE in moderate to severe COPD. Clinicians should suspect VTE in patients who present with dyspnea and should consider possibilities other than infection as causes of COPD exacerbation.

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Section: Discussionsupporting

confidence: 92%

Risk Factors for Venous Thromboembolism in Chronic Obstructive Pulmonary Disease

Kim¹,

Goel²,

Gangar³

et al. 2014

J COPD F

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“…When considering COPD exacerbation, the prevalence of PE seems to differ between patients that require hospitalization and those who do not. According to the 2009 meta-analysis [8], the prevalence of PE in patients with exacerbated COPD ranges from 3.3% when evaluated in an emergency department [9] to 19-29% in outpatients and inpatients [10,11] reaching a maximum of 25-29% in patients requiring hospitalization [3,12]. In our study, subgroup analysis shows that VTE tended to be more frequent in COPD patients that required ICU hospitalization compared to those who were hospitalized in the pneumology ward (respectively, 20.5% vs. 9.8%, NS) but this assertion remains to be confirmed regarding the conflicting data recently published on PE prevalence in patients hospitalized in medical centers: 8% in a Korean population [13] versus 18% in an Israelite population [14].…”

Section: Discussionmentioning

confidence: 99%

“…CT scans were performed to detect unsuspected PE but not used to assess COPD diagnosis. COPD severity was determined according to the criteria of the American Thoracic Society (2006 GOLD score) [7,8]. Severe exacerbation requiring hospitalization was defined as acute COPD deterioration with persistent respiratory clinical symptoms despite repeated bronchodilatators nebulisations delivered in the emergency room or as acute COPD deterioration with severity criteria (respiratory frequency >30/min, heart rate >120/min, cyanosis, systolic arterial pressure <90 mmHg, SpO 2 <90% and/or pH<7.35).…”

Section: Study Groupmentioning

confidence: 99%

Pulmonary Embolism in Patients Hospitalized for Exacerbated COPD and Wheezing

Woimant¹

2015

J Pulm Respir Med

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“…Conversely, the initial syncopal episode and the in-hospital recurrence of sudden respiratory failure despite appropriate therapy for exacerbation of a COPD were suggestive of an episode of acute PE. COPD is associated with an increased risk for PE [9]. ACS is an uncommon complication in patients with an acute episode of PE.…”

Section: Discussionmentioning

confidence: 99%

Atypical case of acute coronary syndrome due to coronary-pulmonary steal syndrome secondary to pulmonary embolism

et al. 2010

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on chronic oxygen therapy due to chronic obstructive pulmonary disease (COPD) in the setting of a bronchiectasic disease, referred to our hospital in September 2009 because of a micturition-nocturnal-syncope preceded by dizziness. The patient had neither a personal history of coronary artery disease nor known cardiovascular risk factors. In the emergency department (ED) the patient presented preserved consciousness and mild dyspnea despite low flows of inhalatory O 2 (2 l/min); chest examination was characterized by sibilant and sonorous rales in addition to bibasilar thin crackles; hemo-gas analysis (HGA) showed severe hypoxemic-hypercapnic acidosis (pH 7.18, pCO 2 85 mmHg, pO 2 58 mmHg, sO 2 84%, HCO 3 -23.5, 5); the ECG demonstrated sinus tachycardia, mild and non-specific ST segment elevation V1-V3; the chest X-ray study showed a COPD pattern, right-basal paracardiac radio-opacity, enlargement of the left cardiac chambers. Blood tests demonstrated a leukocytosis with a mild elevation of LDH and D-Dimer [WBC 19,860, Hb 13.4 g/dL, creatinine 0.85 mg/dL, troponin I (T I ) 0.02 ng/mL, CPK e CPK-MB ns, D-Dimer 678 mg/dL, BNP 37 pg/mL]. In the ED, the patient was started on inhalatory salbutamol, furosemide, steroids and empiric i.v.antibiotic-therapy with piperacillin/tazobactam. An HGA executed 2 h later, documented resolution of the acidosis and of the hypoxia, clear reduction of the pCO 2 (pH 7.4, pO 2 70 mmHg, pCO 2 55 mmHg, sO 2 95%). In the afternoon, the patient was transferred to the department of Internal Medicine. About 1 h after admission, he presented sudden, severe shortness of breath and diaphoresis, the ECG demonstrated sinus tachycardia, a new onset of mild ST segment elevation V3-V6; an HGA showed severe respiratory hypoxic-hypercapnic acidosis (pH 7.16 pCO 2 91 mmHg, pO 2 56 mmHg, sO 2 79%). IV steroids and inhaled salbutamol were again administered with subsequent resolution of the dyspnea and improvement of gas exchange. Blood tests revealed a mild, initial increase of T I (0.77 ng/mL at time 0 min, 0.17 ng/mL 6 h later) with persistently normal LDH, AST, and CK. The ECG presented giant and symmetrical negative T-waves in inferiorlateral derivations (D1-D3, V4-V6). Preliminary diagnosisDr. Squizzato, Prof. Ageno: After cardiologic consultation, on the basis of the ECG abnormalities and a positive marker for myocardial necrosis, therapy with ASA, nitrates and a therapeutic dose of low molecular weight heparin was started. The cardio-thoracic examination was unchanged. A trans-thoracic echocardiogram revealed a mild eccentric left ventricular hypertrophy; a wellpreserved global and segmentary wall-motion (ejection fraction 60%); an altered diastolic function with a pseudonormalized pattern at color-Doppler and tissue-Dopplerimaging; an absence of tricuspidal regurgitation and a normal systolic pulmonary artery pressure; a high-resistance Doppler flow pattern in the first tract of pulmonary

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Prevalence of Pulmonary Embolism in Acute Exacerbations of COPD

Cited by 263 publications

References 22 publications

Risk Factors for Venous Thromboembolism in Chronic Obstructive Pulmonary Disease

Risk Factors for Venous Thromboembolism in Chronic Obstructive Pulmonary Disease

Pulmonary Embolism in Patients Hospitalized for Exacerbated COPD and Wheezing

Atypical case of acute coronary syndrome due to coronary-pulmonary steal syndrome secondary to pulmonary embolism

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